1. Prof. M.C. Bansal
MBBS ., MS., MICOG . , FICOG.
Fonder principal & Control, Jhalwar Medical College & Hospital
Jhalawar
Ex principal & Controller MGMC & Hospital Sitapura ., Jaipur.

2. intra vascular coagulation is linked with three
different interrelated systems.
1. Coagulation System .
2. Coagulation Inhibitory System .
3. Fibrinolytic System .

3.  Hemostasis means prevention of blood loss
after blood vessel is severed or ruptured.
 It is achieved by a complex mechanism .
1, Vascular constriction.
2, Formation of Platelet plug .
3, Clot formation by coagulation process
switched on by trauma,
4, Eventual fibrosis in clot closed to the hole
in blood vessel.

4.  It is brought about by --
a. Local auto acid factor released from
traumatized tissue .,
b. spontaneous and its own Spasm of
myofibrils of blood vessel.
c . Nervous reflex ---traumatized sensory
nerve endings convey to higher center and
efferent nerves carry action orders to
myofibrils .
d. Thromboxane A produced by Platelets .

5.  Small holes are immediately closed by platelet plugs.
 Platelet Cytoplasm has many active factors like Actin,
myocine molecules , thromboplastin , Adenoplasmin
Reticulum , Golgi apparatus ( synthesize Various enzymes
and store Ca ++ ), Mitochondria and enzyme system
capable to produce ATP, ADP , Prostgandins , fibrin
stabilizing factor and growth factor.
 Growth factor growth of and repair of vascular
endothelium myofibrils and fibroblasts needed for blood
vessel repair.
 Platelet membrane is coated with glycoprotein which
prevent their adherence to healthy endothelium .but once
endothelium is damaged the platelets quickly and
abundantly adhere to damaged endothelium and exposed
collegen fibers in the vessel wall there by plugging the
hole / defect.
 Platelet membrane also contain phospholipids.

6. It starts to develop with in 15-20 seconds of
injury to blood vessel .
clotting process activating substances are released
from traumatized tissue , vascular
endothelium, platelets and plasma proteins.
If vascular hole is small , it is plugged with in 2-3
minutes but in case of large defect it may take 20
minutes to 1 hour .
The clot formed in damaged followed by repaired site
retracts and further closes the vessel.
Platelets also play an important role in clot retraction .


11.  Once the clot is formed , blood vessel defect
is repaired the clot is invaded by fibroblasts (
promoted by Growth factor produced by
platelets ) . This continues till complete
organization of clot in to fibrous tissue is
completed with in 1-2 weeks .
 Extra vagated blood is also clotted similarly
and is dissolved by fibrinolysis activity.

13.  The smoothness of vascular endothelium
prevents platelet adhesion and contact
activation of intrinsic clotting cascade.
 A layer of Glycocalyx on endothelium repels
platelets and intrinsic factor to contact .
 Protein bound to endothelium called
Trombomodulin binds with Thrombin and slows
the process of clotting and their complex
molecule “ Thrombomodulin-thrombin “
activates protein C ., inhibits factor V and VIII.

14.  In damaged / rough endothelium –Glycocalyx and
Thrombomodulin is lost hence both factor XII, platelet
adhesion and intrinsic factor initiate the clotting cascade .
 Anti Coagulants are also present in blood itself ----They
remove thrombin from the blood.
1 Fibrin fibers .
2 Alpha globulin also called antithrombin III or antithrombin
Co factor. This prevents excessive clot formation .
3 free Thrombin combines with fibrin fibers and anti
thrombin III , so free thrombin is no more available to
fibrinogen to form fibrin clot
.Heparin –secreted by mast cells , its physiological role is
limited and insignificant , but pharmacological use is very
common in clotting disorders in clinical practice.

15.  Plasma proteins contain euglobin called Plasminogen
when activated changes into Plasmin ( Fibrinlysin ) . It
is proteolytic like trypsin enzyme .
 It digests fibrin fibers , fibrinogen , factor V , VIII , IX
and prothrombin , causing dissolution of clot .
 After few days of trauma when bleeding is stopped
, repair work / healing process starts Endothelium
librates a powerful activator called tissue plasminogen
activator (t-PA ) , which converts plasminogen in to
plasmin to remove the undesired clot to facilited neo
vascularisation and patency of blood vessel necessary
for tissue perfusion .

16. Test Value
Bleeding Time – Duke’s Method 1-3 Mins
Ivy’s Method 1-9 Mins
Coagulation Time- Wright’s Tube Method 3-7 Mins
Lee & White’s Methods 4-9 Mins
Clot Observation Test (Weiner’s) 6-12 Mins
Clot Retraction Time 30 Mins
Fibrindex Or Thrombin Test Formation Of A Clot In 1 Min
Prothrombin Time 11-17 Mins
Thrombin Time 10-15 Secs
Platelet Count 1.5-4 Lacs/Cumm
Fibrin Degeneration Products 0-5 Micro G/Ml
Euglobin Clot Lysis Time 2-4 Hours
Fibrinogren 300-600 Mg%
D-dimer 0-200 Mg/Ml

17. Test Method Of Collection Of Amount Of Blood
Blood In Test Tube / Vial
Hb% Or PCV EDTA Vial 2 Ml
ABO & Rh Group Plain (Clotted) And 3.8% 2 Ml & Few Drops
Sodium Citrate Solution
Vdrl Plain (Clotted) 2ml
Direct / Indirect Coomb’s Plain (Clotted) 2ml
Test
Prothrombin Time 0.5 Ml Of 3.8 % Sodium 4.5 Ml
Citrate Solution
Fibrinogen EDTA Vial 2ml
Platelet EDTA Vial 2ml
Edp Special Tubes Supplied
With Kits
Eclt Citrate Solution 4.5 Ml
D-dimer EDTA Vial 2 Ml

18.  Deficiency of one / more blood clotting
factors .
 Vit. K . Deficiency .
 Hemophillia .
 Thrombocytopenia.
 Liver disease ==not able to produce clotting
factors .
 DIC

19.  Abnormal that develops in blood vessel being
loosely attached may get detached and flow
in circulation –get lodged at distance is called
Embolus ( in pulmonary or aortic circulation -
--chocks the end arteries).the affected area /
organ does not get O2 resulting in Acute
Ischemia and infarction .

20.  Roughened breeched endothelium in blood
vessels ---arteriosclerosis , atheroscerosis
, infection , traumatic .
 Blood flow is very slow or stagnant .
 Intra venous therapy cannulatios left in situ for a
longer time , trombophlebitis .
 Intravenous thrombosis ----Central sinus vein
, deep veins of calf and pelvis .
 Intramural thrombus in heart chambers .
 Its incidences increases in pregnancy
, puerperium LSCS ( hyper coagulability state of
pregnancy , tissue trauma, inflammation
, dehydration , prolong bed rest ) , pelvic surgery